Three forms of MC?

[tex]

Okay, that clarifies it. I thought that you were aware that proctitis can be caused by gluten, (provided the patient is gluten sensitive, of course).

This is a WAEG, but I would assume that antibody production would begin as soon as the body detects the gliadins that trigger gluten sensitivity. IOW, this will begin to happen as soon as the digestive process proceeds far enough to expose these gliadins to the mucosa of the GI tract, which normally should occur in the duodenum, IOW the first third of the small intestine. Antibody production should continue, anywhere the mucosa is exposed to the gliadins.

The antibody production should originate in the epithelial layer of the mucosa, where they will make their way into the bloodstream, to be carried all over the body. The inflammation should only occur in the mucosa, however, at the sites of exposure, since that's where the antibodies will find the information they need to trigger a reaction.

Tex

[mle_ii]

Okay, that clarifies it. I thought that you were aware that proctitis can be caused by gluten, (provided the patient is gluten sensitive, of course).

This is a WAEG, but I would assume that antibody production would begin as soon as the body detects the gliadins that trigger gluten sensitivity. IOW, this will begin to happen as soon as the digestive process proceeds far enough to expose these gliadins to the mucosa of the GI tract, which normally should occur in the duodenum, IOW the first third of the small intestine. Antibody production should continue, anywhere the mucosa is exposed to the gliadins.

The antibody production should originate in the epithelial layer of the mucosa, where they will make their way into the bloodstream, to be carried all over the body. The inflammation should only occur in the mucosa, however, at the sites of exposure, since that's where the antibodies will find the information they need to trigger a reaction.

Tex

Excellent, thanks Tex! I assumed there was a link, but now I finally understand it. Well at least as much as I can at this time. :)

What has me wondering though is why more damage isn't done to the colon/rectum in Celiac patients. Like I said, it appears that the potential for damage would be greater given the transit time in the colon.

Perhaps colon transit time is faster in celiac folks, perhaps once they are diagnosed celiac little is done about investigating damage to the colon, perhaps the villi are more suseptable to damage than the tissues of the colon, perhaps us MC folks were abducted by aliens and had bread sticks shoved up our a.... oh did I write that down... ;) LOL

[tex]

I've wondered that myself, (why they don't show colonic inflammation, but presumably, celiacs don't have a gene that sets them up for the inflammation reaction in the colon, instead they have one or both of the celiac genes, that results in villous atrophy. Of course, it's possibly to have both diseases, (and both types of markers, of course).

Tex

[mle_ii]

Is this another version of MC?

http://jcp.bmjjournals.com/cgi/content/ ... t/55/2/138

Journal of Clinical Pathology 2002;55:138-140

CASE REPORT

Cryptal lymphocytic coloproctitis: a new phenotype of lymphocytic colitis?
C A Rubio and J Lindholm
Department of Pathology, Karolinska Hospital, 171 76 Stockholm, Sweden

Correspondence to:
Dr CA Rubio, Gastrointestinal and Liver Pathology Research Laboratory, Karolinska Institute, 171 76 Stockholm, Sweden;
Carlos.Rubio@onkpat.ki.se

ABSTRACT
Background/Aims: Lymphocytic colitis is a clinicopathological entity characterised by protracted watery diarrhoea and an increased number of intraepithelial lymphocytes (IELs) in the surface epithelium of the colonic mucosa. This report describes two patients with symptoms similar to those of lymphocytic colitis and an increased number of IELs, but within the cryptal epithelium.

Methods: The numbers of IELs were assessed in colorectal biopsies from the two patients. Sections were stained immunohistochemically for CD3, CD8, CD20, and TIA1.

Results: The colorectal biopsies had an abnormally high number of IELs in the epithelium of the crypts but not in the surface epithelium. The IELs in the crypts were CD3+++, CD8+, TIA1+, and CD20-.

Conclusions: The histological diagnosis in these two patients was cryptal lymphocytic coloproctitis. Patients with similar symptoms and an increased number of IELs in the surface epithelium are now filed at this department as having surface lymphocytic coloproctitis. Immunohistochemistry showed that the cryptal IELs were cytotoxic suppressor T cells. Interestingly, a case of cryptal lymphocytic colitis was recently recorded in a non-human primate dying after years of protracted chronic diarrhoea. It is possible that antigens present in the lumen of the crypts elicit a lymphocytic reaction within the cryptal cells.

[tex]

Well, in a way it is, but it appears to be just a subtype of LC, so I presume that's how they would classfy it. Interesting.

Tex

[harvest_table]

It's interesting, all the subtypes and atypical types of MC.

Please correct me, or add to this. Now, after Mikes link we have a possible 6 types of Microscopic Colitis

Collagenous Colitis
Lymphocytic Colitis
Microscopic Colitis, with giant cells
Collangenous Enterocolitis
Lymophocytic Enterocolitis
and possibly Cyptal Lymphocytic coloproctitis


Other than CC or LC has anyone been DX with any of these? In otherwords, my question is do these subtypes have a special test or biopsy that results in a DX other than CC or LC that specifies in writing any of the subtypes of MC?

Love,
Joanna

[tex]

The markers of all these forms are visable under the microscope, so the diagnosis is dependent on the patologists knowledge, and/or discretion. At least thats the way I see it.

I'm pretty sure that most pathologists are not even aware of most of these variations, that's why you don't see any diagnoses showing up. You can't diagnosis something that you're not aware of.

Love,
Tex

[mle_ii]

The markers of all these forms are visable under the microscope, so the diagnosis is dependent on the patologists knowledge, and/or discretion. At least thats the way I see it.

I'm pretty sure that most pathologists are not even aware of most of these variations, that's why you don't see any diagnoses showing up. You can't diagnosis something that you're not aware of.

Love,
Tex

Agreed! And in my case since no biopsies (hell they didn't even look) were taken of my small intestines they could not make the diagnosis of Enterocolitis.

[harvest_table]

Some more light reading on atypical MC & substypes.

http://www.thedoctorsdoctor.com/disease ... .htm#histo

Love,
Joanna

[harvest_table]

The recognition and characterization of microscopic colitis has markedly changed the approach to the evaluation and management of chronic diarrhea. The histologic features of collagenous and lymphocytic colitis are well known to most pathologists. By considering the clinical history and symptoms, the pathologist should be able to reach the correct diagnosis in most cases. However, the spectrum of morphologic changes associated with watery diarrhea syndrome appears to be broader than originally thought. Morphologic changes more often associated with chronic inflammatory bowel disease or even chronic ischemic or infectious colitis have been noted in patients with clinically established microscopic colitis. The data presented in this article suggest that microscopic colitis is a heterogeneous entity, which includes both classic and "atypical" forms. Problems arise when cases do not fit the usual pattern or lack some of the findings that are expected. Pathologists should be aware of the presence of atypical forms of microscopic colitis.

It's so interesting (not surprising) that patients with established MC have shown morphologic changes more often associated with IBD, chronic ischemic or infectious colitis.

I'm not sure I understand this when it states that MC is a heterogeneous entity that includes both the classic (LC&CC) and atypical forms. Since the definition of heterogeneous means varied, mixed, assorted, diverse and such are they suggesting that one could be DX with CC or LC as well as an atypical form at the same time? IOW, are CC and LC sometimes comprised of the classic and atypical types at the same time? Do they exist together?

I'm thinking to much....better go pull some weeds.

Love,
Joanna

[tex]

Hi Joanna,

I would interpret that statement to mean that they are simply pointing out that MC can be present in any one of several different forms. As far as I am aware, only one type can be present at any given time, though one form can segue into another, and back again, at any time, (IOW, CC can turn into LC, and vice versa, but if markers for both are present, then it is simply called MC, not CC and LC, for example).

Love,
Tex

[harvest_table]

Thanks Tex, that clarifies it for me. It's facinating reading about the atypical and subtypes of MC. Also interesting how it intermingles with IBD. Somehow I missed your previous conversations on Sallys board- it's complicated. No wonder it's called the trickster disease!

Love,
Joanna

[tex]

Yes it is complicated, and it's interesting how we are all similarly affected, and yet it affects each of us differetly.

Love,
Tex

[mle_ii]

Just so that I'm clear. I thought that MC/LC/CC was classified as an IBD, or is it not?

Thanks,
Mike

[harvest_table]

Mike,

Believe it's an IBD. Surely someone will correct me if I'm wrong.

Love,
Joanna